A red blood cell mismatch between a mother’s blood and their fetus causes hemolytic disease in new-born. This will result in serious complications and can even lead to fatality. With the proper use of immunoprophylaxis during the gestation period, deadly outcomes from this illness can be prevented.  However, early detection and treatment play a pivotal role in avoiding the catastrophic effects of this condition. The counseling of pregnant females has been made mandatory so that new-born do not face this harmful illness. Dr. Louis K. Diamond initially documented the hemolytic illness of the fetus and infant in 1932.HDFN is an immune-mediated red blood cell (RBC) condition in which maternal antibodies react with foetal or neonatal RBCs. HDFN can result in considerable morbidity and mortality, particularly in areas with poor healthcare facilities. 

The effects of HDFN are:


Hydrops fetalis



In the past decade, the incidence and prevalence of HDFN have dropped dramatically due to early detection, therapy, and prevention.

Maternal antibodies target fetal or neonatal RBC antigens through two major mechanisms:

Incompatibility with ABO

Hemorrhage in the womb of the mother

ABO incompatibility is a congenital blood type mismatch between the mother and the fetus. All immunization caused by fetomaternal hemorrhage (FMH), on the other hand, is an acquired immune-mediated mechanism that frequently impacts later pregnancies rather than the one in which the FMH occurs.


Antigens in fatal blood that are foreign to maternal blood are inherited from paternal genes. For instance, an Rh-negative mother can have an Rh-positive fetus due to her partner being Rh-positive. Antibodies that create because of FMH put resulting pregnancies in danger for HDFN as the primary antibodies to create are of IgM type, which can’t cross the placenta. Maternal antibodies quickly produce IgG antibodies in response to further exposures to the Rh-D antigen, and these antibodies do pass the placenta.

Infants suffer hemolytic anemia as their RBCs are attacked and broken down. Bilirubin is produced when heme is broken down and is eliminated in utero by the placenta. The liver begins processing the bilirubin at the time of birth. Utilizing the enzyme uridine diphosphate-glucuronosyltransferase, indirect bilirubin, also known as unconjugated bilirubin, is converted to direct bilirubin (UDP-glucuronosyltransferase). The conjugated bilirubin is excreted in bile, where it is excreted in feces and urine.

In infants, especially preterm infants, liver processing is less efficient, which often leads to natural physiologic jaundice


If the hemolytic disease of the fetus and newborn is identified or suspected in utero, medical assistance should be taken as early as possible in the pregnancy. Affected pregnancies can be managed by monitoring antibody titers and fetal middle cerebral artery velocities, intrauterine transfusions and possibly early delivery as infants with severe anemia may not tolerate term labor well.

Hemolytic infection of the infant is overseen by treating hyperbilirubinemia with phototherapy and exsanguination transfusion if necessary. Routine all-inclusive screening with transcutaneous bilirubin (TcB) frequently happens within 24 hours of life, yet screening ought to be directed when hyperbilirubinemia is thought. An elevated TcB should always be verified with a serum total bilirubin (TB). The level of bilirubin in the infant’s blood is then risk categorized using the hour-specific Bhutani nomogram. Depending on the Infant’s level of risk, this nomogram offers a suggested cut-off point for beginning phototherapy versus early transfusions.